Evidence map›Paper›PMID 24947041›Full record

ArticleCancer research2014

IL4 receptor ILR4α regulates metastatic colonization by mammary tumors through multiple signaling pathways.

Katherine T Venmar, Kathy J Carter, Daniel G Hwang, E Ashley Dozier, Barbara Fingleton

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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  15. Interleukin-4 treatment reduces leukemia burden in acute myeloid leukemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Katherine T VenmarDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Kathy J CarterDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Daniel G HwangDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
E Ashley DozierDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Barbara FingletonDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee. barbara.fingleton@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Epithelial IL4Ralpha Regulates Colon Tumor ProgressionR01CA157781 · NCI · VANDERBILT UNIVERSITY · PI FINGLETON, BARBARA · 2011 to 2015
$1.6M
NCATS NIH HHS 2 UL1 TR000445-06NCATS NIH HHS UL1 TR000445NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA157781NCI NIH HHS R01CA157781NCRR NIH HHS UL1 RR024975NCRR NIH HHS UL1 RR024975-01NIGMS NIH HHS 5T32GM008554NIGMS NIH HHS T32 GM008554
6 · The paper itself

Abstract

IL4, a cytokine produced mainly by immune cells, may promote the growth of epithelial tumors by mediating increased proliferation and survival. Here, we show that the type II IL4 receptor (IL4R) is expressed and activated in human breast cancer and mouse models of breast cancer. In metastatic mouse breast cancer cells, RNAi-mediated silencing of IL4Rα, a component of the IL4R, was sufficient to attenuate growth at metastatic sites. Similar results were obtained with control tumor cells in IL4-deficient mice. Decreased metastatic capacity of IL4Rα "knockdown" cells was attributed, in part, to reductions in proliferation and survival of breast cancer cells. In addition, we observed an overall increase in immune infiltrates within IL4Rα knockdown tumors, indicating that enhanced clearance of knockdown tumor cells could also contribute to the reduction in knockdown tumor size. Pharmacologic investigations suggested that IL4-induced cancer cell colonization was mediated, in part, by activation of Erk1/2, Akt, and mTOR. Reduced levels of pAkt and pErk1/2 in IL4Rα knockdown tumor metastases were associated with limited outgrowth, supporting roles for Akt and Erk activation in mediating the tumor-promoting effects of IL4Rα. Collectively, our results offer a preclinical proof-of-concept for targeting IL4/IL4Rα signaling as a therapeutic strategy to limit breast cancer metastasis.

Indexed as

AnimalsBreast NeoplasmsCell Growth ProcessesCell Line, TumorFemaleHumansInterleukin-4 Receptor alpha SubunitLiver Neoplasms, ExperimentalLung NeoplasmsMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm MetastasisSignal TransductionInterleukin-4 Receptor alpha Subunit

Identifiers

PMID24947041
PMCPMC4134711
OpenAlexW2029376715

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.